OBJECTIVES: 1. To elucidate cerebral metabolic responses of perinatal animals to hypoglycemia and to recovery from hypoglycemia. 2. To ascertain the relationship of cerebro-spinal fluid glucose to blood glucose during (a) hypoglycemia, (b) hypoglycemia reversed by glucose treatment and (c) hyperglycemia. 3. To establish in hypoglycemic newborn animals the hypoxic threshold below which cerebral metabolic derangements occur. 4. To determine whether oxidative substrates other than glucose protect the from metabolic disturbances during hypoglycemia comined with hypoxia. 5. To ascertain possible residual residual acute and long-term cerebral consequences of hypoxia. 6. To clarify the role of hyperglycemia in the pathogenesis of hypoxia brain damage. METHODS: 1. Measurements of cerebral blood flow, glucose consumption and oxidative metabolism in newborn rats and dogs during hypoglycemia and during recovery. 2. Measurements of cerebrospinal fluid glucose in relation to fluctuations (hypoglycemia or hyperglycemia) in blood glucose. 3. Determination of mortality and acute and long-term neurophathological morbidity in newborn animals subjected to graded hypoglycemia combined with graded hypoxia. 4. Determination of the protective influence of oxidative substrates other than glucose during periods of hypoglycemia combined with hypoxia. Clarification of the role of hyperglycemia in the pathogenesis of hypoxic brain damage. SIGNIFICANCE: To gain insight into the usefulness of monitoring cerebral function in hypoglycemic and hypoxic infants and to suggest improved modes of therapy.